Profiling of miRNAs in pediatric asthma: Upregulation of miRNA-221 and miRNA-485-3p

被引:87
作者
Liu, Feng [1 ]
Qin, Hou-Bing [1 ]
Xu, Bing [2 ]
Zhou, Hui [3 ]
Zhao, De-Yu [1 ]
机构
[1] Nanjing Med Univ, Nanjing Childrens Hosp, Dept Resp Med, Nanjing 210029, Jiangsu, Peoples R China
[2] Shanghai Jiao Tong Univ, Affiliated Peoples Hosp 6, Dept Emergency, Shanghai 200233, Peoples R China
[3] Nanjing Med Univ, Nanjing Matern & Child Hlth Hosp, Nanjing 210004, Jiangsu, Peoples R China
关键词
miRNA; pediatric asthma; pathogenesis; CHILDHOOD ASTHMA; MICRORNAS; HYPERRESPONSIVENESS; AIRWAYS; DISEASE; CELLS;
D O I
10.3892/mmr.2012.1030
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The aim of this study was to investigate the expression profiles of microRNAs (miRNAs) in pediatric asthma and to determine candidate miRNAs responsible for the pathogenesis of this disease. Microarrays were used to detect the differences in the miRNA expression levels between asthmatic children and controls. Airway inflammation was evaluated by cell counting and tissue biopsy in an ovalbumin (OVA)-induced murine asthma model. Real-time polymerase chain reaction (PCR) was used to verify the differentially expressed miRNAs. The targets of the identified miRNAs were analyzed by bioinformatic analysis. The sprouty-related protein with an EVH1 domain-2 (Spred-2) protein content was assessed by western blotting. Differences were observed in the expression of miRNAs between the asthmatic children and controls. Upregulation of miRNA-221 and miRNA-485-3p in pediatric asthmatics and murine asthma models were verified by real-time PCR. Spred-2, a predicted target of miRNA-221 and miRNA-485-3p, was downregulated in murine asthma models. Upregulation of miRNA-221 and miRNA-485-3p may regulate the pathogenesis of asthma.
引用
收藏
页码:1178 / 1182
页数:5
相关论文
共 20 条
[1]   The functions of animal microRNAs [J].
Ambros, V .
NATURE, 2004, 431 (7006) :350-355
[2]   MicroRNAs: Genomics, biogenesis, mechanism, and function (Reprinted from Cell, vol 116, pg 281-297, 2004) [J].
Bartel, David P. .
CELL, 2007, 131 (04) :11-29
[3]   The global burden of asthma [J].
Braman, Sidney S. .
CHEST, 2006, 130 (01) :4S-12S
[4]   MicroRNAs and Their Therapeutic Potential for Human Diseases: MiR-133a and Bronchial Smooth Muscle Hyperresponsiveness in Asthma [J].
Chiba, Yoshihiko ;
Misawa, Miwa .
JOURNAL OF PHARMACOLOGICAL SCIENCES, 2010, 114 (03) :264-268
[5]   The development of allergic inflammation [J].
Galli, Stephen J. ;
Tsai, Mindy ;
Piliponsky, Adrian M. .
NATURE, 2008, 454 (7203) :445-454
[6]   MicroRNAs Profiling in Murine Models of Acute and Chronic Asthma: A Relationship with mRNAs Targets [J].
Garbacki, Nancy ;
Di Valentin, Emmanuel ;
Huynh-Thu, Van Anh ;
Geurts, Pierre ;
Irrthum, Alexandre ;
Crahay, Celine ;
Arnould, Thierry ;
Deroanne, Christophe ;
Piette, Jacques ;
Cataldo, Didier ;
Colige, Alain .
PLOS ONE, 2011, 6 (01)
[7]   Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness [J].
Inoue, H ;
Kato, R ;
Fukuyama, S ;
Nonami, A ;
Taniguchi, KI ;
Matsunmoto, K ;
Nakano, T ;
Tsuda, M ;
Matsumura, M ;
Kubo, M ;
Ishikawa, F ;
Moon, BG ;
Takatsu, K ;
Nakanishi, Y ;
Yoshimura, A .
JOURNAL OF EXPERIMENTAL MEDICINE, 2005, 201 (01) :73-82
[8]   A systematic review and meta-analysis of interventions used to reduce exposure to house dust and their effect on the development and severity of asthma [J].
MacDonald, Clare ;
Sternberg, Anna ;
Hunter, Paul R. .
ENVIRONMENTAL HEALTH PERSPECTIVES, 2007, 115 (12) :1691-1695
[9]   The global burden of asthma: executive summary of the GINA Dissemination Committee Report [J].
Masoli, M ;
Fabian, D ;
Holt, S ;
Beasley, R .
ALLERGY, 2004, 59 (05) :469-478
[10]   Antagonism of microRNA-126 suppresses the effector function of TH2 cells and the development of allergic airways disease [J].
Mattes, Joerg ;
Collison, Adam ;
Plank, Maximilian ;
Phipps, Simon ;
Foster, Paul S. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2009, 106 (44) :18704-18709